Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

In this study, we showed a clinical correlation between adiponectin and VEGF-C as well as tumor stage in human chondrosarcoma tissues. We further demonstrated that adiponectin promoted VEGF-C expression and secretion in human chondrosarcoma cells. The conditioned medium from adiponectin-treated cells significantly induced tube formation and migration of human lymphatic endothelial cells. In addition, adiponectin knockdown inhibited lymphangiogenesis in vitro and in vivo. We also found that adiponectin-induced VEGF-C is mediated by the CaMKII, AMPK and p38 signaling pathway. Furthermore, the expression of miR-27b was negatively regulated by adiponectin via the CaMKII, AMPK and p38 cascade. Our study is the first to describe the mechanism of adiponectin-promoted lymphangiogenesis by upregulating VEGF-C expression in chondrosarcomas. Thus, adiponectin could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis.

Source: Clinical Science - May 31, 2016 Category: Biomedical Science Authors: Huang, C.-Y., Chang, A.-C., Chen, H.-T., Wang, S.-W., Lo, Y.-S., Tang, C. H. Tags: PublishAheadOfPrint Source Type: research